Abstract
FOXA1 is associated with malignant tumors, but the function of FOXA1 in EOC is unclear. HDAC3 can influence the proliferation, migration and invasion ability of EOC. In this study, we wanted to explore the function of FOXA1 in ovarian cancer and the relationship between HDAC3 and FOXA1.The expression of HDAC3 and FOXA1 was detected by immunohistochemical staining of primary lesions from 127 epithelial ovarian carcinoma patients. A proliferation assay, a Transwell assay, an apoptosis assay and animal experiments were used to assess the proliferation, invasion and apoptosis abilities of ovarian cancer cells before and after transfection with FOXA1. The relevance of the in vitro findings was confirmed in xenografts. The H-scores for FOXA1 and HDAC3 staining in FIGO stage III-IV were noticeably higher and predicted adverse clinical outcomes in patients with ovarian cancer. The expression level of HDAC3 was significantly correlated with the expression level of FOXA1. Invasion, proliferation and apoptosis capacity and tumor formation were decreased in the FOXA1-knockdown cells. Experiments in xenografts confirmed that HDAC3 mediated tumor formation. In conclusion, FOXA1 can be modulated by HDAC3 through the Wnt/β-catenin signaling pathway, and FOXA1 plays essential roles in the proliferation, apoptosis and invasion of EOC cell lines and xenograft experiments.
Highlights
Epithelial ovarian carcinoma (EOC) is one of the leading causes of cancer-related death among women, accounting for 195,000 new cases and 185,000 deaths annually worldwide [1]
Histone deacetylase 3 (HDAC3) is a member of the histone deacetylase family that is associated with cellular physiological functions, such as signal transduction, cell cycle, proliferation, apoptosis, and cardiac development
We explored the relationship of helpHistone deacetylase 3 (HDAC3) and FOXA1 in EOC and the function of FOXA1 in EOC progression through in vitro and in vivo assays
Summary
Epithelial ovarian carcinoma (EOC) is one of the leading causes of cancer-related death among women, accounting for 195,000 new cases and 185,000 deaths annually worldwide [1]. Patients with a poor prognosis may have early tumor metastasis, drug resistance and recurrence [3, 4]. Histone deacetylase 3 (HDAC3) is a member of the histone deacetylase family that is associated with cellular physiological functions, such as signal transduction, cell cycle, proliferation, apoptosis, and cardiac development. HDAC3 plays an important role in the progression of malignant tumors, especially in proliferation [5], apoptosis [6], metastasis [7], angiogenesis [8] and anticancer drug resistance [9]. We discovered that HDAC3 can influence the proliferation, migration and invasion ability of EOC [10]. Tumor progression is a complex pathophysiological process, and HDAC3 alone cannot control biological behavior. Further studies are necessary to investigate the HDAC3-related proteins
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